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ischemic arrhythmia
相关语句
  缺血性心律失常
     Antagonism of BQ 610 on acute myocardial ischemic arrhythmia in cats
     BQ_(610)对猫急性缺血性心律失常的拮抗作用
短句来源
     Results: BQ 610 dose dependently antagonized the acute ischemic arrhythmia.
     结果:BQ610呈剂量依赖性拮抗LAD结扎引起的猫急性缺血性心律失常
短句来源
     The Inhibitory Effect of BN3C on Ischemic Arrhythmia in Anesthetized Rats
     BN3C抗麻醉大鼠缺血性心律失常的作用
短句来源
     Endothelin-1 10-23 Deoxyribozyme: Design and Study of the Effects on Acute Ischemic Arrhythmia in Isolated Rat Hearts
     内皮素-1 10-23脱氧核酶的构建及其抗急性缺血性心律失常的实验研究
短句来源
     Baroreflex Sensitivity May Predict Severity oF Ischemic Arrhythmia in Rats
     大鼠压力反射敏感性可预测缺血性心律失常严重程度
短句来源
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  “ischemic arrhythmia”译为未确定词的双语例句
     Methods Sixty patients with ischemic arrhythmia were randomly divided into A group treated with Wenxinkeli(27g/d)and B group treated with Wenxinkeli(27g/d)and atorvastain(10mg/d).
     方法将60例患者随机分为A组与B组,A组给予稳心颗粒(27g/d),B组给予稳心颗粒联合阿托伐他汀(10mg/d)。
短句来源
     It was found that pretreatment with SA 13.3 and 15mg/kg iv diminished significantly infarction at 4h after ligation,SA prevented ischemic arrhythmia.
     实验发现SA13.3和15mg/kg于冠状动脉结扎前iV,显著降低结扎后4h的心肌梗塞范围,降低死亡率。
短句来源
     SA 10.6, 13.3 and 15mg/kg iv decreased markedly the early ischemic arrhythmia in conscious rats.
     SA13.3和15mg/kg显著缩小心肌梗塞范围,降低血清LDH含量,减轻清醒大鼠缺血早期心律失常。
短句来源
     Amiodarone 7.5mg·kg-1 had the same effects on the prevention of ischemic arrhythmia.
     胺碘酮7.5mg/kg有类似作用。
短句来源
     Conclusion: Ginkgolide B had protective effect on ischemic myocardium to prevent ischemic arrhythmia.
     结论 :银杏苦内酯B可对抗心肌缺血所引起的心肌电生理的变化 ,提示银杏苦内酯B可预防心律失常的发生。
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  相似匹配句对
     Effects of lysophosphatidylcholine in ischemic arrhythmia
     溶血磷脂胆碱在缺血性心律失常中的作用
短句来源
     Therefore,VVP and chances of ischemic arrhythmia decreased.
     心肌缺血后心室易损期(VVP)明显延长 34± 2 2 .6 1ms,迷走神经刺激后VVP明显缩短至 11.75± 7.72m
短句来源
     Propafenone on arrhythmia
     普罗帕酮治疗儿童心肌病心律失常疗效观察
短句来源
     Arrhythmia on swallowing
     吞咽时引起心律失常(附3例报告)
短句来源
     Group 2-ischemic;
     ②缺血(ischemiC)组;
短句来源
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  ischemic arrhythmia
The result clewed that mechanism of PD156707 to reduce acute ischemic arrhythmia may be related to scavenge of oxygen free radical.
      
Finally, early ischemic arrhythmia may also be viewed in the light of contraction-excitation feedback.
      


The effects of Sinomenine on experimental arrhythmia were studied. The result showed that Sinomenine could shorten the arrhythmetic period induced by picrotoxin in rabbit and protect rat against arrhythmia induced by BaCl_2. Sinomenine was found to recover the arrhythmia induced by BaCl_2-Ach into sinus rhythm in mice, Beside these Sinomenine also showed significant antagonising to ischemic arrhythmia.

本实验研究了青藤碱对实验性心律失常的作用。实验结果表明,青藤碱可缩短印防己毒素诱发家兔心律失常的持续时间;具有对抗BaCl_2诱发大鼠和CaCl_2-Ach诱发小鼠心律失常的作用;能使印防己毒素、BaCl_2、CaCl_2-Ach所致心律失常复转为窦性心律。并对缺血性心律失常有明显的对抗作用。

A recirculating nonpulsatile perfusion circuit was used in isolated rabbit hearts. Furyl-dihydropyridine Ⅰ( 2, 6 - dimethyl - 4 - furyl - 1, 4 - dihydropyridine-3, 5-dicarboxylate)20μmol/L was shown to inhibit the release of creatine phosphokinase (CPK) and α-hydroxybutyrate dehydrogenase (HBD) from myocardium, decrease myocardial calcium and sodium contents by 5.3±1.1μmol/g dry weitght (P<0.01, n=6) and 1.50±0.17mmol/g dry weight (P<0.05, n=6) from 8.3±1.1μmol/g dry weight and 1.96±0.32 mmol/g dry weight respectively....

A recirculating nonpulsatile perfusion circuit was used in isolated rabbit hearts. Furyl-dihydropyridine Ⅰ( 2, 6 - dimethyl - 4 - furyl - 1, 4 - dihydropyridine-3, 5-dicarboxylate)20μmol/L was shown to inhibit the release of creatine phosphokinase (CPK) and α-hydroxybutyrate dehydrogenase (HBD) from myocardium, decrease myocardial calcium and sodium contents by 5.3±1.1μmol/g dry weitght (P<0.01, n=6) and 1.50±0.17mmol/g dry weight (P<0.05, n=6) from 8.3±1.1μmol/g dry weight and 1.96±0.32 mmol/g dry weight respectively. It was alse found to reduce coronary resistance and increase coronary flow of the ischemic myocardium, and prevent ischemic arrhythmia, thereby limit myocardial injury during regional ischemia in isolated rabbit hearts.

呋喃二氢吡啶Ⅰ20μmol╱L能使离体兔心局部缺血心肌肌酸磷酸激酶(CPK)和α-羟丁酸脱氢酶(HBD)的释放量明显减少;冠脉阻力下降,流量增加;并能降低血浆及心肌中钙、钠含量,预防缺血性心律失常的发生。提示该药对离体兔心缺血心肌的保护作用,与降低缺血心肌细胞钙、钠含量有关。

Ischemia-mimic solution (hypoxia, hyperkalemia, acidosis, no substrate) in-duced changes of transmembrane potential and ionic current were observed in24 sheep cardiac Purkinje fibers. The sequence of changes of transmembranepotential was as follows: Two to three min after perfusion with ischemiamimicsolution, the maximum diastolie potential (MDP) was depolarized slightly, andattended by a decrease of depolarization rate of phase 4 while the action potentialduration (APD) was shortened or underwent a shortening-prolongation-reshor-tening...

Ischemia-mimic solution (hypoxia, hyperkalemia, acidosis, no substrate) in-duced changes of transmembrane potential and ionic current were observed in24 sheep cardiac Purkinje fibers. The sequence of changes of transmembranepotential was as follows: Two to three min after perfusion with ischemiamimicsolution, the maximum diastolie potential (MDP) was depolarized slightly, andattended by a decrease of depolarization rate of phase 4 while the action potentialduration (APD) was shortened or underwent a shortening-prolongation-reshor-tening process. Then, the plateau of action potential disappeared gradually. AsMDP was depolarized further, the action potential amplitude (APA) and the excit-ability of the Purkinje fibers decreased continuously until action potential could nolonger be elicited. The whole process took 30min to 160min in different preparations. When the APD was shortened, the instantaneous outward current was alwaysincreased at all membrane potential levels. The steady-state current-voltagerelationship (CVR) curve was changed from S shape to a straight line, and theinward rectification phenomenon disappeared. Under ischemic condition, theamplitude of I_(si) was decreased from 6.74±4.48 nA to 0.86±1.39 nA, and theCVR curve shifted more to the negative. The above results indicate that under the ischemic condition, the pacemakerfunction of cardiac Purkinje cell is inhibited, a large amount of K~+ ions outflowsand inward current I_(si) is decreased. These changes may be the reasons for thegenesis of ischemic arrhythmia.

以低氧、高钾、低pH、无能量供应的模拟缺血溶液灌流离体绵羊心脏浦肯野纤维,观察“缺血”对心肌跨膜电位和离子流的影响。实验共24例。跨膜电位的变化过程如下:模拟缺血液灌流后2-3min,首先出现最大舒张电位(MDP)轻度除极,4期舒张除极速率减慢,随后动作电位时程(APD)缩短(n=13)或先缩短、后延长、再缩短的变化(n=11),平台逐渐消失,最后MDP进一步除极,动作电位波幅(APA)减小,兴奋性逐渐降低,以致不能引出动作电位(AP)。其中6例即使MDP高于-60mV时AP已不能引出。以上变化过程历时长短不等,在不同标本为30-160min。跨膜离子流方面,当APD缩短时,在所有膜电位水平即时外向电流都明显增加。稳态电流-电压关系曲线由正常的S形变成直线,内向整流现象消失。慢内向离子流由“缺血”前的6.74±4.48nA减少到0.86±1.39nA,(M±SD,P<0.01,n=8),在多数测试电位水平都有显著减少,其电流-电压关系曲线向较负电位方向移位。以上结果提示:心肌“缺血”时浦肯野细胞起搏功能受抑制,细胞内大量K~+外流,Ca~(2+)内流减少,心肌细胞除极,以上多种变化可能为心肌缺血时心律失常发生...

以低氧、高钾、低pH、无能量供应的模拟缺血溶液灌流离体绵羊心脏浦肯野纤维,观察“缺血”对心肌跨膜电位和离子流的影响。实验共24例。跨膜电位的变化过程如下:模拟缺血液灌流后2-3min,首先出现最大舒张电位(MDP)轻度除极,4期舒张除极速率减慢,随后动作电位时程(APD)缩短(n=13)或先缩短、后延长、再缩短的变化(n=11),平台逐渐消失,最后MDP进一步除极,动作电位波幅(APA)减小,兴奋性逐渐降低,以致不能引出动作电位(AP)。其中6例即使MDP高于-60mV时AP已不能引出。以上变化过程历时长短不等,在不同标本为30-160min。跨膜离子流方面,当APD缩短时,在所有膜电位水平即时外向电流都明显增加。稳态电流-电压关系曲线由正常的S形变成直线,内向整流现象消失。慢内向离子流由“缺血”前的6.74±4.48nA减少到0.86±1.39nA,(M±SD,P<0.01,n=8),在多数测试电位水平都有显著减少,其电流-电压关系曲线向较负电位方向移位。以上结果提示:心肌“缺血”时浦肯野细胞起搏功能受抑制,细胞内大量K~+外流,Ca~(2+)内流减少,心肌细胞除极,以上多种变化可能为心肌缺血时心律失常发生的原因。

 
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